The heart is the center of a person's circulatory system. It includes an electro-mechanical system performing two major pumping functions. The left portions of the heart draw oxygenated blood from the lungs and pump it to the organs of the body to provide oxygen. The right portions of the heart draw deoxygenated blood from the organs and pump it to the lungs where the blood is oxygenated. These pumping functions result from contractions of the myocardium, or heart muscle. In a normal heart, the sinoatrial node, the heart's natural pacemaker, generates electrical impulses that propagate through an electrical conduction system to various regions of the heart and excite the myocardial tissues of these regions. In a normal electrical conduction system, coordinated delays in the propagations of the electrical impulses cause the various portions of the heart to contract in synchrony to provide efficient pumping functions. A blocked or otherwise abnormal electrical conduction and/or deteriorated myocardial tissue can cause dysynchronous contraction of the heart. The dysynchrony can be characterized as an arrhythmia, which can further be characterized as bradycardias, tachycardias, automaticity, re-entry arrhythmias, and fibrillation, among others. The existence of an arrhythmia can result in poor hemodynamic performance and diminished blood supply.
Ischemia is a condition where a portion of a body is deprived of adequate oxygen and metabolite removal due to an interruption in blood supply caused by an occlusion of a blood vessel. One example of ischemia is cardiac ischemia. It follows then that cardiac ischemia is a condition in which the myocardium is deprived of adequate oxygen and metabolite removal due to an interruption in blood supply, such as resulting from an occlusion of a coronary artery.
Myocardial infarction (MI) is the necrosis of portions of the myocardial tissue resulted from cardiac ischemia. The necrotic tissue, known as infarcted tissue, loses the contractile properties of the normal, healthy myocardial tissue. Consequently, the overall contractility of the myocardium is weakened, resulting in an impaired hemodynamic performance. Following an MI, cardiac remodeling starts with expansion of the region of infarcted tissue and progresses to a chronic, global expansion in the size and change in the shape of the entire left ventricle. The consequences include a further impaired hemodynamic performance and a significantly increased risk of developing heart failure, as well as a risk of suffering recurrent MI.